The defects of immune function which result in human autoimmune disorders are widely believed to be caused or mediated by changes in functional subsets of T-lymphocytes. The ability to study such changes has been hampered by a lack of adequate means to identify and isolate these subpopulations. Based on the well studied murine Ly antigen system, observations with rare allo- and xenoantisera and on functional and theoretical considerations, it should be possible to differentiate T-lymphocyte subpopulations by antigenic differences. Using somatic cell hybridization to produce hybrids between murine plasmacytomas and immune spleen cells, we will produce "hybridomas" secreting monoclonal antibodies to human T-lymphocytes. In analogy to the murine Ly antigens, some of the hybridoma clones should secrete antibodies to helper, suppressor and effector T-lymphocytes. These clones will be selected on the basis of an extensive screening protocol. The monoclonal reagents produced by the clones will be tested for subset specificity and ability to define the function of subsets in vitro, using tests allowing assessment of helper, suppressor and effector cell function. Relevant monoclonal reagents will then be used to assess the status of particular regulator functions in patients with rheumatoid arthritis, systemic lupus erythematosis and Hodgkins disease.